Gallstones are an odd phenomenon. Despite being exceptionally common, affecting between 10-15% of the U.S. population, pinpointing the causes of gallstones has been elusive. Older age, being female and overweight/obese increase the likelihood of developing gallstones, a process that develops over decades. Because most gallstones are composed largely of cholesterol, doctors have blamed high cholesterol as the cause for gallstone formation, but that notion is proving—as with all other issues surrounding cholesterol—to be an oversimplification. This, in addition to the fact that fat consumption, while it does not cause gallstone formation, can unmask their presence, since fat digestion requires bile and a stone that becomes lodged in the bile duct causes acute gallbladder pain to develop, has unfortunately caused many doctors to conflate the two phenomena and advise people with gallstones to consume a low-fat, low-cholesterol diet. This awful advice remains common today despite several studies demonstrating that reducing fat or calories actually causes gallstone formation.
It is likely that wheat and related grains are a contributor to gallstone formation via several routes. The lectin, wheat germ agglutinin, is known to block the hormone cholecystokinin, or CCK. When ingested food contacts the duodenum, CCK is released that, in turn, provokes the gallbladder to contract and expel bile through the bile duct to emulsify fats and provokes the pancreas to release pancreatic enzymes to digest fats, proteins, and carbohydrates. When wheat germ agglutinin is in the vicinity, from, say, a sandwich, bagel, or breakfast cereal, CCK is blocked. One consequence is inadequate release of bile from the gallbladder, a situation that cultivates bile stasis, i.e., bile that accumulates in the gallbladder and encourages crystal formation that leads to gallstones. Wheat germ agglutinin, by the way, is found in wheat, rye, barley, and rice, all with identical structures. There may be other means by which wheat and related grains cultivate gallstone formation, but that remains speculative, factors such as direct intestinal inflammation caused by wheat germ agglutinin and changes in bowel flora due to impaired digestion from lack of adequate bile and pancreatic enzymes.
There is also growing appreciation that gallstones contain multiple species of bacteria and may therefore represent yet another manifestation of dysbiosis, disrupted bowel flora. The microorganisms recovered from people with acute gallbladder attacks and cholecystitis (and even from gallstones themselves, even in the absence of overt infection) are typically Escherichia coli, Klebsiella, Enterobacter, Pseudomonas, Citrobacter—i.e., the Gram-negative Enterobacteriaceae species that dominate in SIBO. And, because the bile duct empties into the duodenum, the uppermost portion of small intestine, it suggests that the dysbiosis that cultivates gallstone formation must be in the form of small intestinal bacterial overgrowth, SIBO. If dysbiosis were confined to the colon, it likely would not reach the duodenum. It therefore stands to reason that a full-length dysbiosis must be present in order to reach the duodenum.
A recent analysis demonstrated that the bacterial composition of stool from people with gallstones is different from healthy people without gallstones, specifically enriched in Enterobacteriaceae, and that the bacterial composition of both gallstones and bile in people with stones is unique, with an even greater proportion of Enterobacteriaceae as well as Ruminococcaceae, Bacteroidales, and Clostridiales. Some have therefore speculated that the change in bacterial composition in the gallbladder and biliary tree leads to supersaturation of bile with cholesterol crystals, promoting stone formation. It is not yet possible to declare that dysbiosis/SIBO causes or contributes to gallstone formation or whether it is a consequence, but growing evidence is pointing towards SIBO as a fundamental and necessary contributor.
It is a tangle, no doubt, but one that is gradually becoming untangled. We await better answers, but until then, we can still derive a few take-home messages. If you have gallstones, you should strongly consider:
- Banishing all wheat and grains, i.e., sources of wheat germ agglutinin that blocks gallbladder contraction and cultivates bile stasis, as well as intestinal inflammation and dysbiosis. Of course, if you do not yet have gallstones, removing all wheat and grains from the diet yields enormous health benefits, including not blocking CCK and impaired digestion.
- Explore the question of SIBO–which has become enormously easier with availability of the AIRE device for H2 breath detection. (Join our frequent Undoctored Inner Circle conversations about use of the AIRE for detection, tracking during antibiotic therapy, and to assess for recurrence. Alternatively, sign up for my in-depth 4-part SIBO Workshop, discounted for paid Wheat Belly Blog subscribers, that shows how to manage SIBO on your own without the doctor.) The ability to measure breath hydrogen gas is a game-changer for intestinal health. You can also appreciate that, if SIBO was the cause for gallstones, removing the gallbladder does nothing to address the cause.
- Not limiting dietary fat. We do not limit fat on the Wheat Belly lifestyle but enjoy fatty cuts of meat, butter, coconut oil, etc. This remains true even if you have had your gallbladder removed. If any fat intolerance is encountered after gallbladder removal, e.g., diarrhea or abdominal discomfort with fat ingestion, first think SIBO, not lack of bile. The bacterial species of SIBO impair fat digestion. (The only people who can benefit by limiting fat are those with active gallbladder disease in whom fat digestion can provoke gallbladder attacks.) Limiting dietary fat can reduce symptoms, but does not address the cause, not to mention raises triglycerides that lead to heart disease, cultivates fatty liver, raises blood sugar and pushes you closer to type 2 diabetes. Limiting dietary fat is a very destructive practice and yields no benefits for gallbladder or bile health, nor do the majority of people without a gallbladder need to supplement bile or pancreatic enzymes if SIBO is addressed.